Environmental factors and aryl hydrocarbon hydroxylase activity (CYP1A1 phenotype) in human lymphocytes.
Since aryl hydrocarbon hydroxylase (AHH) is considered to be responsible for the activation of benzo(a)pyrene (BP) and other polyaromatic hydrocarbons in cigarette smoke to carcinogens, it is important to examine AHH activity in the determination of susceptibility to lung cancer. Lymphocytes from healthy male adults (239) of non-smokers and smokers were cultured in vitro and assayed for non-induced and 3-methylcholanthrene (MC)-induced AHH activity and AHH inducibility (MC-induced AHH activity/non-induced AHH activity). A day-to-day variation in AHH activity was not observed while a seasonal variation was apparent. Very wide differences in non-induced AHH and MC-induced AHH activities were observed. The association of some selected environmental factors and AHH activity was studied. Age was related to non-induced AHH activity (Spearman's rank correlation coefficients (r), r = 0.185, p < 0.005) and AHH inducibility (r = -0.329, p < 0.001). Coffee consumption was associated with non-induced (age-adjusted r = 0.138, p < 0.05) and MC-induced AHH activity (age-adjusted r = 0.173, p < 0.01). Cigarette smoking was correlated with non-induced AHH activity (age-adjusted r = 0.191, p < 0.005) and AHH inducibility (age-adjusted r = -0.191, p < 0.005). No significant association was observed for any other selected factors, including alcohol intake or broiled food consumption. In conclusion, AHH activity might be affected by cigarette smoking and coffee consumption, and was dependent on the age of the donor. Day-to-day and seasonal variation analyses showed that this assay method was reproducible and reliable and AHH inducibility might be a useful biomarker in cancer epidemiology. As those factors may affect the AHH activity, a careful control of those factors to AHH activity is necessary in epidemiological studies on the association between AHH inducibility in human lymphocytes and lung cancer.
Kiyohara
C
C
Department of Public Health, School of Medicine, Kyushu University, Fukuoka, Japan.
Hirohata
T
T
D000328:Adult; D001189:Aryl Hydrocarbon Hydroxylases / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D002273:Carcinogens; D002478:Cells, Cultured; D019363:Cytochrome P-450 CYP1A1 / Q000235:genetics*; D004790:Enzyme Induction; D006801:Humans; D008175:Lung Neoplasms / Q000453:epidemiology / Q000209:etiology*; D008214:Lymphocytes / Q000201:enzymology*; D008297:Male; D008748:Methylcholanthrene; D010641:Phenotype; D012044:Regression Analysis; D012307:Risk Factors; D012907:Smoking
D002273:Carcinogens; D008748:Methylcholanthrene; D001189:Aryl Hydrocarbon Hydroxylases; D019363:Cytochrome P-450 CYP1A1